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HYDROCEPHALUS
Vitya Chandika

2013-061-060

Priscila Stevanni 2013-061-066

Pricilia Nicholas

2013-061-070

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Definition

Abnormal accumulation
of CSF due to disturbance
of flow, formation or
absorption.

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Function of CSF

As a brain cushion, a shock absorber for brain and

spinal cord.

Circulates nutrients.

Removes waste product.

Maintain ionic hemostasis

Production rate: 0.2 0.35 ml/min

Total volume: 120ml

Lateral Ventricle

Foramina Monro

3rd ventricle

Aquaductus Sylvii

4th Ventricle
Foramina Luschka &
Magendie
Cisterns system

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EPIDEMIOLOGY
Estimated
Incidence

prevalence: 1-1.5%
of congenital hydrocephalus is 0.9-

1.8/1000 births

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ETIOLOGY
Congenital

Chiari Type 2 malformation and/or myelomeningocele (MM)

Chiari Type 1 malformation: HCP may occur wituh 4th

ventricle outlet obstruction

Primary aqueductal stenosis

Secondary aqueductal gliosis

Dandy Walker malformation: atresia of foramina of Luschka

& Magendie

X-linked inherited disorder

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ETIOLOGY
Acquired

Infectious

Post meningitis

Cysticercosis

Post hemorrhagic

Post SAH

Post IVH (intraventricular hemorrhage)

Secondary to masses

Non-neoplastic: e.g. vascular malformation

Neoplastic

Post-op

Neurosarcoidosis

Constitutional ventriculomegaly: asymptomatic. Needs no treatment

Associated with spinal tumors

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CLASSIFICATION
Obstructive

Block proximal to the arachnoid

granulation (AG). On CT/MRI: Enlargement of

ventricles proximal to block
Tumors
Blood

clots

Congenital

malformation

Arachnoiditis
Stenosis

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CLASSIFICATION
Communicating

CSF circulation

block at level of AG
Intraventricular
Subarachnoid
Meningitis

hemorrhage

hemorrhage

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SPECIAL FORMS
Pseudohydrocephalus

Hydrocephalus ex vacuo

Otitic hydrocephalus

External hydrocephalus

Hydranencephaly

Normal

pressure hydrocephalus

Entrapped
Arrested

fourth ventricle

hydrocephalus

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Pathophysiology

stenosis
+ Aqueductal
The most common cause of congenital
hydrocephalus(43%)
-Aqueduct develops about the 6th week of gestation
-M:F = 2:1
-Prognosis: 11-30% mortality

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Pathophysiology
Dilated temporal & frontal horn, often
asymetry, results:
-Elevation of corpus callosum
-Stretching / perforation of septum pellucidum
-Thinning of cerebral mantle
-Enlargement of third ventricle downward into
fossa pituitary

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CLINICAL MANIFESTATION
In

young children

Increasing head circumference

Full fontanel

Sutural diastasis

Irritable

hyperactive reflexes

Vomit

Setting sun appearance

Thin scalp with dilated veins

Macewens sign: cracked pot sound on percussing

over dilated ventricles

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CLINICAL MANIFESTATION
In

older children/adults

Papilledema

Hypertension

Nausea / vomiting

Gait changes

Upgaze and/or abducens palsy

Incontinence

Bradycardia

Apnea

Dementia

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CT scan / MRI
Criteria:
Size of both temporal horns (TH) 2 mm in width
(in the absence of HCP, the temporal horns should be barely
visible)
and
The sylvian & interhemispheric fissures and cerebral sulci are
not visible

OR

Both TH are 2 mm
and the ratio

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CT scan / MRI
Suggestive of hydrocephalus:

1.

Mickey Mouse ventricles

2.

Sagital MRI may show thinning and/or upward

bowing of the corpus callosum

3.

Ratio

4.

Evans index:

CT scan

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Treatment

Diuretics
For premature infants
-Acetazolamide (carbonic anhydrase inhibitor)
~25mg/kg/day PO divided TID,
increase 25mg/kg/day each day until 100mg/kg/day is
reached
-Simultaneously start furosemide: 1mg/kg/day PO divided
TID

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Treatment
Lumbal

puncture / Spinal taps

only for communicating Hydrocephalus,

Normal Pressure Hydrocephalus

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Surgical
choroid

plexectomy

eliminating
third

the obstruction

ventriculostomy

Shunting

(VP/VA)

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THANKYOU